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Emerging and spreading zoonoses are major concerns among the public and public health professionals. Recognition, surveillance, and reporting are our first line of defense.
DR. MOELLERING is Shields Warren-Mallinckrodt Professor of Medicine, Harvard Medical School; and chairman of the department ofmedicine, division of infectious diseases, Beth Israel Deaconess Medical Center, Boston, Mass.
DR. SEJVAR is a neuroepidemiologist, division of viral and rickettsial diseases, Centers for Disease Control and Prevention, Atlanta, Ga.DR. STEERE is professor of medicine, Harvard Medical School, and director of rheumatology, Massachusetts General Hospital, Boston.
MS. ASCH-GOODKIN is a contributing editor for Contemporary Pediatrics.Dr. Moellering is a consultant for Roche and GlaxoSmithKline. Drs. Sejvar and Steere and Ms. Asch-Goodkin have nothing to disclose inregard to affiliations with, or financial interests in, any organization that may have an interest in any part of this article, which is adaptedfrom Patient Care, an Advanstar publication.
A new zoonosis is characterized by signs and symptoms that are distinct from those of previously recognized zoonoses: Existing tolerance to the zoonosis decreases, occurrence goes from rare to common, the nature of the illness changes from mild to severe, or cases cluster in a location or social group. A new zoonosis may be identified when a population is examined using more effective surveillance capabilities and improved diagnostic techniques.
New zoonoses are often identified because of better health records, rapid global communication systems (the Web, e-mail, and television, for example), and better diagnostic methods (such as monoclonal and polyclonal antibody techniques, enzyme-linked immunosorbent assays [ELISA], and polymerase chain reaction [PCR] testing).
First identified approximately 30 years ago in Lyme, a small town in Connecticut, Lyme disease is now found throughout New England and the Mid-Atlantic states, as well as Wisconsin, Minnesota, and northern California. It is caused by the spirochete Borrelia burgdorferi transmitted by the deer tick (Ixodes scapularis in the Northeast and Midwest and Ixodes pacificus in the West). By now, most pediatricians who practice in endemic areas have seen patients and parents concerned about a tick bite or presenting with erythema migrans (EM)-a bull's-eye rash-the most common presentation of early localized disease.
Bites from nymphal deer ticks, which are usually prevalent in early summer, are largely responsible for transmission of the disease. The tick must be attached to the skin for 24 to 36 hours before the spirochete is transmitted; the probability that a nymphal tick bite will lead to Lyme disease is low in patients who have removed the deer tick soon after it has attached. In highly endemic areas, when an engorged I scapularis tick is attached for at least 48 hours, prophylaxis with a single dose of doxycycline is reasonable in adults and children at least 8 years old.1
Lyme disease should be considered in a patient who lives in or who has recently visited the Lyme belt and who presents with EM. The rash is often accompanied by arthralgia, fatigue, fever, headache, malaise, or myalgia. Some patients may present with these symptoms during summer, without EM. Because serologic testing is often negative in early disease, a 2- to 3-week course of amoxicillin or doxycycline is recommended in patients with EM, without serologic testing being performed.2
Early disseminated disease may include multiple EM lesions, cranial nerve palsy, lymphocytic meningitis, migratory joint and muscle pains, myocarditis, radiculoneuritis, and transient atrioventricular blocks of varying degree. Objective neurologic abnormalities, with the possible exception of facial palsy alone, warrant a month-long course of IV antibiotics. High-degree AV block is treated initially with IV antibiotics that can be switched to oral therapy once heart block improves.
The most common manifestation of late Lyme disease is intermittent or chronic monoarticular or oligoarticular arthritis affecting large joints, typically the knees. This manifestation of Lyme disease can usually be successfully treated with oral antibiotics, although IV treatment is sometimes necessary. Consultation with a rheumatologist can be helpful. A small percentage of patients may develop a chronic axonal polyneuropathy or encephalopathy late in the illness.
When EM is not present, the diagnosis of Lyme disease should be confirmed by serologic testing, following a positive ELISA test result with a Western blot test.3 Clinical findings, exposure in an endemic area, and the presence of antibodies contribute to the diagnosis of Lyme disease.
Treatment is usually successful, with neurologic and arthritic sequelae receding in weeks or months, although some patients may complain of continued pain, sleeplessness, fatigue, or cognitive impairment for many months or years. This post-Lyme disease syndrome may be indistinguishable from fibromyalgia or chronic fatigue syndrome and is equally difficult to treat. Two controlled trials have demonstrated conclusively that repeated and prolonged courses of antibiotics are no more effective than placebo.4 Positive serologic test results often persist after antibiotic treatment and do not prove active infection. Simply validating the reality and severity of the patient's symptoms is often helpful.5